Background:MicroRNA-24 (miR-24) plays an important role in heart failure by reducing the efficiency of myocardial excitation-contraction coupling.Prolonged cardiac hypertrophy may lead to heart failure,but little is known about the role of miR-24 in cardiac hypertrophy.This study aimed to preliminarily investigate the function of miR-24 and its mechanisms in cardiac hypertrophy.Methods:Twelve Sprague-Dawley rats with a body weight of 50 ± 5 g were recruited and randomly divided into two groups:a transverse aortic constriction (TAC) group and a sham surgery group.Hypertrophy index was measured and calculated by echocardiography and hematoxylin and eosin staining.TargetScans algorithm-based prediction was used to search for the targets of miR-24,which was subsequently confirmed by a real-time polymerase chain reaction and luciferase assay,Immunofluorescence labeling was used to measure the cell surface area,and 3H-leucine incorporation was used to detect the synthesis of total protein in neonatal rat cardiac myocytes (NRCMs) with the overexpression of miR-24.In addition,flow cytometry was performed to observe the alteration in the cell cycle.Statistical analysis was carried out with GraphPad Prism v5.0 and SPSS 19.0.A two-sided P ＜ 0.05 was considered as the threshold for significance.Results:The expression ofmiR-24 was abnormally increased in TAC rat cardiac tissue (t =-2.938,P＜ 0.05).TargetScans algorithm-based prediction demonstrated that CDKN 1B (p27,Kip 1),a cell cycle regulator,was a putative target ofmiR-24,and was confirmed by luciferase assay.The expression of p27 was decreased in TAC rat cardiac tissue (t =2.896,P ＜ 0.05).The overexpression of miR-24 in NRCMs led to the decreased expression of p27 (t =4.400,P ＜ 0.01),and decreased G0/G1 arrest in cell cycle and cardiomyocyte hypertrophy.Conclusion:MiR-24 promotes cardiac hypertrophy partly by affecting the cell cycle through down-regulation of p27 expression.